No description available.

No description available.

Pregnancy is a state of many hormonal changes that can make interpretation of thyroid function tests difficult. Measuring trimester-specific reference values of thyrotropin and free thyroxine is recommended. Because overt maternal hypothyroidism negatively affects the fetus, timely recognition and treatment are important. Women taking levothyroxine prepregnancy require a ≤50% dose increase during pregnancy. Hyperthyroidism can result from excessive human chorionic gonadotropin or Graves disease. Radioactive scanning should be avoided during pregnancy. Antithyroidal drug therapy should consist of propylthiouracil during the first trimester and methimazole thereafter. If indicated, beta blockers can be administered under obstetrical supervision. Iodine deficiency is a known goitrogen and stimulus for thyroid nodular growth. Thyroid nodules may enlarge, but the incidence of thyroid cancer is not increased during pregnancy. Suspicious nodules should be biopsied and, if necessary, removed during the second trimester; otherwise, follow-up can safely be conducted postpartum. Thyroid-stimulating hormone suppression for any preexisting thyroid cancer or suspicious nodules should achieve free or total T4 in the upper normal range for pregnancy. Postpartum thyroiditis occurs more frequently in antithyroid peroxidase-positive women, who should be screened by measuring serum thyrotropin at 6 to 12 weeks' gestation and at 3 and 6 months postpartum.

Kidney disease and pregnancy may exist in two general settings: acute kidney injury that develops during pregnancy, and chronic kidney disease that predates conception. In the first trimester of pregnancy, acute kidney injury is most often the result of hyperemesis gravidarum, ectopic pregnancy, or miscarriage. In the second and third trimesters, the common causes of acute kidney injury are severe preeclampsia, hemolysis-elevated liver enzymes-low platelets syndrome, acute fatty liver of pregnancy, and thrombotic microangiopathies, which may pose diagnostic challenges to the clinician. Cortical necrosis and obstructive uropathy are other conditions that may lead to acute kidney injury in these trimesters. Early recognition of these disorders is essential to timely treatment that can improve both maternal and fetal outcomes. In women with preexisting kidney disease, pregnancy-related outcomes depend upon the degree of renal impairment, the amount of proteinuria, and the severity of hypertension. Neonatal and maternal outcomes in pregnancies among renal transplant patients are generally good if the mother has normal baseline allograft function. Common renally active drugs and immunosuppressant medications must be prescribed, with special considerations in pregnant patients.

Blastomycosis rarely presents in pregnancy. Pregnancy is a state of partial immunodeficiency that predisposes to blastomyces infection, especially in endemic areas. Blastomycosis in pregnancy has been reported in a few female patients and their offspring. We are reporting a 32-year-old pregnant patient at 34 weeks of gestation who presented with a lung mass. The cytopathological exam of the biopsy taken by fine needle aspiration showed evidence of Blastomyces organisms. She received Liposomal Amphotericin B and was followed closely until delivery. The placenta was examined and did not show evidence of infection in the fetus. Healthcare professionals in endemic areas such as Tennessee should be aware of blastomycosis in pregnancy.

No description available.

The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are widely used as cholesterol lowering agents that have an acceptable safety profile. As a group, this class of drugs has been associated with few immunologic reactions. Simvastatin (Zocor) has been linked to three cases of drug-induced lupus-like syndrome. We report the case of an additional patient who developed pleurisy and arthralgia after he started taking this low-density lipoprotein and cholesterol-lowering agent.

Cicatricial pemphigoid is an unusual mucocutaneous disease that is characterized by subepidermal blister formation involving the oral and conjunctival membranes. The oral lesions are expressed as erythema and induration and have rarely been associated with upper airway obstruction. We report the case of a patient with dyspnea and an abnormal flow-volume loop who was found to have subglottic compromise due to cicatricial pemphigoid. Immunosuppressive therapy improved his symptoms and air flow.

No description available.

In this study, we demonstrate that killer cell lectin-like receptor subfamily G member 1 (KLRG1), a transmembrane protein preferentially expressed on T cells, is highly expressed on CD56+ NK cells, which are significantly reduced in their numbers and functions in the peripheral blood of patients with chronic hepatitis C virus (HCV) infection compared to subjects without infection. KLRG1 expression is also upregulated on healthy NK cells exposed to Huh-7 hepatocytes infected with HCV in vitro. Importantly, the expression levels of KLRG1 are inversely associated with the capacity of NK cells to proliferate and to produce gamma interferon (IFN-γ) but positively associated with apoptosis of NK cells in response to inflammatory cytokine stimulation. KLRG1- NK cells, including CD56bright and CD56dim subsets, exhibit impaired cell activation and IFN-γ production but increased apoptosis compared to KLRG1- NK cells, particularly in HCV-infected individuals. Importantly, blockade of KLRG1 signaling significantly recovered the impaired IFN-γ production by NK cells from HCV-infected subjects. Blockade of KLRG1 also enhanced the impaired phosphorylation of Akt (Ser473) in NK cells from HCV-infected subjects. Taken together, these results indicate that KLRG1 negatively regulates NK cell numbers and functions via the Akt pathway, thus providing a novel marker and therapeutic target for HCV infection.